The complexities of breast cancer desmoplasia

Walker, Rosemary A.

doi:10.1186/bcr287

Cited by 170 publications

(116 citation statements)

References 21 publications

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“…The desmoplasia that accompanies tumor progression is well characterized (25). Recent studies demonstrate that collagen alignment as well as density can be altered in invasive tumors, and straight, perpendicularly aligned fibers create avenues for cell movement and invasion (41,49,50).…”

Section: Discussionmentioning

confidence: 99%

“…Collagen I is a major component of the extracellular matrix (ECM) in the developing and adult mammary gland and of the increased fibrillar collagens that elevate mammographic density (23,24). As cancers progress, the stiffness of the ECM around the tumor increases (desmoplasia) as a result of altered collagen deposition, crosslinking, and remodeling (25). This increased ECM density increases breast cancer invasiveness in vitro and metastasis in vivo (for reviews, see Refs.…”

Section: Prolactin (Prl)mentioning

confidence: 99%

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Stiff Collagen Matrices Increase Tumorigenic Prolactin Signaling in Breast Cancer Cells

Barcus

Keely

Eliceiri

et al. 2013

Journal of Biological Chemistry

114

121

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Background: Prolactin, but not its best studied mediator STAT5a, is associated with breast cancer progression. Results: In stiff but not compliant collagen matrices, prolactin promotes tumorigenic processes via an enhanced ERK1/2 cascade. Conclusion: Extracellular matrix stiffness powerfully modulates the spectrum of prolactin signals and actions. Significance: Prolactin and stiff matrices interact in a feed-forward loop in breast cancer, suggesting new therapeutic approaches.

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Section: Discussionmentioning

confidence: 99%

Section: Prolactin (Prl)mentioning

confidence: 99%

Stiff Collagen Matrices Increase Tumorigenic Prolactin Signaling in Breast Cancer Cells

Barcus

Keely

Eliceiri

et al. 2013

Journal of Biological Chemistry

114

121

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“…Desmoplasia is also called as desmoplastic reaction, in which a reaction occurs as a secondary response to injury. 18,19 Desmoplastic reactions are associated with the expression of hypoxia-related proteins and metastasis in medullary thyroid carcinoma. 20,21 In PTC, desmoplastic reactions are also accompanied by the expression of hypoxia markers and with invasive behaviour, such as lymph node metastases.…”

Section: Discussionmentioning

confidence: 99%

Implications of oncocytic change in papillary thyroid cancer

Hong

et al. 2016

Clinical Endocrinology

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SummaryObjective Although the presence of oncocytic change in less than 75% of a tumour is not considered to indicate oncocytic variants of papillary thyroid carcinoma (PTC), we frequently observe partial oncocytic change, especially in obese PTC patients. Thus, we sought to investigate the relationship between the presence of oncocytic change of PTC and its prognosis. Design, setting and participants We retrospectively studied 142 patients with PTC who had undergone surgery between 2000 and 2005, and re-evaluated their PTC slides to record the proportion of oncocytic change in 10% increments from 0% to 100%. Major outcome measure We analysed the relationship between the proportion of oncocytic change and clinicopathological prognostic factors. Results Oncocytic change was found in 45Á8% (65/142) of PTC patients. The proportion of patients with oncocytic change was higher in obese patients than in lean patients and showed a significant correlation with the BMI (r = 0Á195, P = 0Á020). The PTC patients with oncocytic change showed a higher recurrence rate than PTC patients without oncocytic change (30Á8% vs 11Á7%, respectively; P = 0Á005). The presence of oncocytic change in PTC patients was associated with a shorter disease-free survival in a Kaplan-Meier analysis after a mean follow-up of 8Á9 years. Conclusion The patients with PTC with oncocytic change presented with a higher recurrence rate and were more likely to be obese. These findings suggest that presence of oncocytic change is a poor prognostic factor in PTC patients, even if the oncocytic change involves less than 75% of a tumour.

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“…Tumor stroma contains many cell types, most important of which are fibroblasts, which, via the secretion of extracellular matrix components, growth factors, and proteases, affect crucially tumor development (1)(2)(3)(4). In many solid tumors, predominately in the breast, carcinomas are characterized by a specific stromal reaction called desmoplasia, often referred to as scirrhous carcinoma (2,5). This reaction is classically described by the proliferation of fibroblasts adjacent to the tumor and the overproduction of extracellular matrix components, mainly collagen.…”

Section: Introductionmentioning

confidence: 99%

Imatinib Mesylate Inhibits Proliferation and Exerts an Antifibrotic Effect in Human Breast Stroma Fibroblasts

Gioni

Karampinas

Voutsinas

et al. 2008

Molecular Cancer Research

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Tumor stroma plays an important role in cancer development. In a variety of tumors, such as breast carcinomas, a desmoplastic response, characterized by stromal fibroblast and collagen accumulation, is observed having synergistic effects on tumor progression. However, the effect of known anticancer drugs on stromal cells has not been thoroughly investigated. Imatinib mesylate is a selective inhibitor of several protein tyrosine kinases, including the receptor of platelet-derived growth factor, an important mediator of desmoplasia. Recently, we have shown that imatinib inhibits the growth and invasiveness of human epithelial breast cancer cells. Here, we studied the effect of imatinib on the proliferation and collagen accumulation in breast stromal fibroblasts. We have shown that it blocks the activation of the extracellular signal-regulated kinase and Akt signaling pathways and up-regulates cyclin-dependent kinase inhibitor p21 WAF1 , leading to the inhibition of fibroblast proliferation, by arresting them at the G 0 /G 1 phase of the cell cycle. Imatinib inhibits more potently the platelet-derived growth factor -mediated stimulation of breast fibroblast proliferation. By using specific inhibitors, we have found that this is due to the inhibition of the Akt pathway. In addition, imatinib inhibits fibroblast-mediated collagen accumulation. Conventional and quantitative PCR analysis, as well as gelatin zymography, indicates that this is due to the down-regulation of mRNA synthesis of collagen I and collagen III-the main collagen types in breast stroma-and not to the up-regulation or activation of collagenases matrix metalloproteinase 2 and matrix metalloproteinase 9. These data indicate that imatinib has an antifibrotic effect on human breast stromal fibroblasts that may inhibit desmoplastic reaction and thus tumor progression. (Mol Cancer Res 2008;6(5):706 -14)

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The complexities of breast cancer desmoplasia

Cited by 170 publications

References 21 publications

Stiff Collagen Matrices Increase Tumorigenic Prolactin Signaling in Breast Cancer Cells

Stiff Collagen Matrices Increase Tumorigenic Prolactin Signaling in Breast Cancer Cells

Implications of oncocytic change in papillary thyroid cancer

Imatinib Mesylate Inhibits Proliferation and Exerts an Antifibrotic Effect in Human Breast Stroma Fibroblasts

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